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Ficolin B in Diabetic Kidney Disease in a Mouse Model of Type 1 Diabetes.

Holt CB, Østergaard JA, Axelgaard E, Nielsen GK, Endo Y, Thiel S, Hansen TK - Mediators Inflamm. (2015)

Bottom Line: The complement system seems to play a key role through erroneous complement activation via hyperglycaemia-induced neoepitopes.Recently mannan-binding lectin (MBL) was shown to worsen diabetic kidney changes.In conclusion, the diabetes-induced effects on kidney weight and ACR were not modified by the presence or absence of ficolin B.

View Article: PubMed Central - PubMed

Affiliation: Department of Endocrinology and Internal Medicine, Aarhus University Hospital, 8000 Aarhus, Denmark ; Department of Biomedicine, Aarhus University, 8000 Aarhus, Denmark.

ABSTRACT

Background: The innate immune system may have adverse effects in diabetes and cardiovascular disease. The complement system seems to play a key role through erroneous complement activation via hyperglycaemia-induced neoepitopes. Recently mannan-binding lectin (MBL) was shown to worsen diabetic kidney changes. We hypothesize that mouse ficolin B exerts detrimental effects in the diabetic kidney as seen for MBL.

Methods: We induced diabetes with streptozotocin in female wild-type mice and ficolin B knockout mice and included two similar nondiabetic groups. Renal hypertrophy and excretion of urinary albumin and creatinine were quantified to assess diabetic kidney damage.

Results: In the wild-type groups, the kidney weighed 24% more in the diabetic mice compared to the controls. The diabetes-induced increase in kidney weight was 29% in the ficolin B knockout mice, that is, equal to wild-type animals (two-way ANOVA, P = 0.60). In the wild-type mice the albumin-to-creatinine ratio (ACR) was 32.5 mg/g higher in the diabetic mice compared to the controls. The difference was 62.5 mg/g in the ficolin B knockout mice, but this was not significantly different from the wild-type animals (two-way ANOVA, P = 0.21).

Conclusions: In conclusion, the diabetes-induced effects on kidney weight and ACR were not modified by the presence or absence of ficolin B.

No MeSH data available.


Related in: MedlinePlus

Kidney weight (a) and kidney weight per body weight (b) depicted for each of the four groups. The black error bars are illustrating mean ± standard deviation for each group. WT: wild-type; KO: ficolin B knockout.
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fig2: Kidney weight (a) and kidney weight per body weight (b) depicted for each of the four groups. The black error bars are illustrating mean ± standard deviation for each group. WT: wild-type; KO: ficolin B knockout.

Mentions: The kidney weight was equally increased in diabetic wild-type mice, 24% (CI: 13%–36%), and in the diabetic knockout mice, 29% (CI: 12%–47%), compared to the respective control groups (Figure 2(a)). No interaction between knockout and diabetes was found (P = 0.60), indicating that wild-type and knockout mice develop the same degree of diabetes-induced renal hypertrophy. The considerable body weight difference between the two diabetic groups at study end indicated that the kidney weight was to be normalised to the body weight. This is illustrated in Figure 2(b). Ficolin B did not modify the diabetes-induced increase in kidney weight when testing for interaction (P = 0.11). Furthermore, no significant statistical difference was found in kidney weight per body weight between the diabetic wild-type, 1.95 mg/g, and the diabetic knockout, 2.89 mg/g (P = 0.09).


Ficolin B in Diabetic Kidney Disease in a Mouse Model of Type 1 Diabetes.

Holt CB, Østergaard JA, Axelgaard E, Nielsen GK, Endo Y, Thiel S, Hansen TK - Mediators Inflamm. (2015)

Kidney weight (a) and kidney weight per body weight (b) depicted for each of the four groups. The black error bars are illustrating mean ± standard deviation for each group. WT: wild-type; KO: ficolin B knockout.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4539181&req=5

fig2: Kidney weight (a) and kidney weight per body weight (b) depicted for each of the four groups. The black error bars are illustrating mean ± standard deviation for each group. WT: wild-type; KO: ficolin B knockout.
Mentions: The kidney weight was equally increased in diabetic wild-type mice, 24% (CI: 13%–36%), and in the diabetic knockout mice, 29% (CI: 12%–47%), compared to the respective control groups (Figure 2(a)). No interaction between knockout and diabetes was found (P = 0.60), indicating that wild-type and knockout mice develop the same degree of diabetes-induced renal hypertrophy. The considerable body weight difference between the two diabetic groups at study end indicated that the kidney weight was to be normalised to the body weight. This is illustrated in Figure 2(b). Ficolin B did not modify the diabetes-induced increase in kidney weight when testing for interaction (P = 0.11). Furthermore, no significant statistical difference was found in kidney weight per body weight between the diabetic wild-type, 1.95 mg/g, and the diabetic knockout, 2.89 mg/g (P = 0.09).

Bottom Line: The complement system seems to play a key role through erroneous complement activation via hyperglycaemia-induced neoepitopes.Recently mannan-binding lectin (MBL) was shown to worsen diabetic kidney changes.In conclusion, the diabetes-induced effects on kidney weight and ACR were not modified by the presence or absence of ficolin B.

View Article: PubMed Central - PubMed

Affiliation: Department of Endocrinology and Internal Medicine, Aarhus University Hospital, 8000 Aarhus, Denmark ; Department of Biomedicine, Aarhus University, 8000 Aarhus, Denmark.

ABSTRACT

Background: The innate immune system may have adverse effects in diabetes and cardiovascular disease. The complement system seems to play a key role through erroneous complement activation via hyperglycaemia-induced neoepitopes. Recently mannan-binding lectin (MBL) was shown to worsen diabetic kidney changes. We hypothesize that mouse ficolin B exerts detrimental effects in the diabetic kidney as seen for MBL.

Methods: We induced diabetes with streptozotocin in female wild-type mice and ficolin B knockout mice and included two similar nondiabetic groups. Renal hypertrophy and excretion of urinary albumin and creatinine were quantified to assess diabetic kidney damage.

Results: In the wild-type groups, the kidney weighed 24% more in the diabetic mice compared to the controls. The diabetes-induced increase in kidney weight was 29% in the ficolin B knockout mice, that is, equal to wild-type animals (two-way ANOVA, P = 0.60). In the wild-type mice the albumin-to-creatinine ratio (ACR) was 32.5 mg/g higher in the diabetic mice compared to the controls. The difference was 62.5 mg/g in the ficolin B knockout mice, but this was not significantly different from the wild-type animals (two-way ANOVA, P = 0.21).

Conclusions: In conclusion, the diabetes-induced effects on kidney weight and ACR were not modified by the presence or absence of ficolin B.

No MeSH data available.


Related in: MedlinePlus